A Practical Approach to Cardiac Anesthesia (Practical Approach Series) 5th Ed.

3 The Cardiac Surgical Patient

Donald E. Martin and Charles E. Chambers


 1. Inability to climb two flights of stairs showed a positive predictive value of 82% for postoperative pulmonary or cardiac complications.

 2. Silent ischemia is more common in the elderly and diabetic patients, with 15% to 35% of all myocardial infarctions (MIs) occurring as silent events.

 3. Isolated asymptomatic ventricular arrhythmias, even nonsustained ventricular tachycardia (VT), have not been associated with complications following noncardiac surgery.

 4. Patients with left bundle branch block and especially with right coronary artery disease in whom a Swan-Ganz catheter is being placed may need availability of a transcutaneous pacemaker because of the risk of inducing right bundle branch block, and thus complete heart block, during passage of the pulmonary artery catheter.

 5. Hypertension with blood pressure lower than 180/110 has not been found to be an important predictor of increased perioperative cardiac risk, but it may be a marker for chronic cardiovascular disease.

 6. The presence of carotid stenosis increases the risk of postoperative stroke from approximately 2% in patients without carotid stenosis to 10% with stenosis of greater than 50%, and to 11% to 19% with stenosis of >80%.

 7. Selective use of pharmacologic perfusion imaging in only patients who have at least one of two clinical risk factors for ischemic disease (age >70 yrs and congestive heart failure) can maximize the usefulness of this procedure in predicting cardiac outcome.

 8. PCI is not beneficial when used solely as a means to prepare a patient with coronary artery disease for surgery.

 9. Elective surgery requiring interruption of anti-platelet therapy should not be scheduled within 1 month of bare metal stent (BMS) placement or within 12 months of drug eluting stent (DES) placement.

10. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers appear to cause perioperative hypotension, so it is prudent to hold these agents the morning of surgery but re-start them as soon as the patient is euvolemic postoperatively.

CARDIOVASCULAR DISEASE IS OUR SOCIETY’S number 1 health problem. According to the most recent CDC data, heart disease alone affects 26.8 million Americans, or about 12% of our population [1]. Of the 34 million Americans hospitalized in 2007, 3.9 million (11.5%) had heart disease. Heart disease remains the leading cause of death in patients greater than age 65, with an age adjusted death rate of 100 per 10,000, or 1%, per year. Furthermore, of the 45 million surgical procedures performed in the United States in 2007, approximately 6.9 million procedures involved the cardiovascular system. 405,000 were coronary artery bypass procedures, which represents a 13% decrease since 2003 and is associated with an increase in the number of percutaneous angioplasties and stents [2]. In contrast, the number of valve procedures has increased, with the number of valve repair procedures growing faster than the number of valve replacements [3]. The prime goals of preoperative evaluation and therapy for cardiac surgical procedures, therefore, are to quantify and reduce the patient’s risk during surgery and the postoperative period.

The factors that are important in determining perioperative morbidity and anesthetic management must be assessed carefully for each patient.

I. Patient presentation

   A. Clinical perioperative risk assessment—multifactorial risk indices

Multifactorial risk indices, which identify and assign relative importance to many potential risk factors, have become increasingly sophisticated over the last three decades and are used with increasing frequency to combine multiple risk factors into a single risk estimate, to determine an individual patient’s risk of morbidity and mortality following heart surgery, to guide therapy, and to “risk adjust” the surgical outcomes of populations. One of the first multifactorial risk scores was developed by Paiement, in 1983 [4], and identified eight simple clinical risk factors:

      1. poor left ventricular function

      2. congestive heart failure

      3. unstable angina or MI within 6 mos

      4. age greater than 65 yrs

      5. severe obesity

      6. reoperation

      7. emergency surgery

      8. severe or uncontrolled systemic illness.

     Recent models still incorporate many of these eight factors.

   The preoperative clinical factors that affect hospital survival following heart surgery have been studied by multiple authors from the 1990s until the present time [3,59]. The initial studies focused on coronary artery bypass grafting (CABG) surgery, but more recent indices have been validated for valvular surgery and combined valve and CABG surgery as well.

   The most important risk factors in these studies are compared in Table 3.1. The earlier indices assigned “point values” to indicate the relative risk of postoperative mortality associated with each preoperative risk factor, usually based on multivariate analysis. More recent studies provide more specific odds ratios of mortality associated with each of a larger number of predictors.

   In 2001, Dupuis and colleagues developed and validated the cardiac risk evaluation (CARE) score, which incorporated similar factors but viewed them more intuitively in a manner similar to American Society of Anesthesiologists (ASA) physical status (Table 3.2) [9]. In 2004, Ouattara and colleagues [11] compared the CARE score to two other multifactorial indices, the Tu score [12] and Euroscore [5]. Their analysis found no difference among these scores in predicting mortality and morbidity following cardiac surgery at that time. However, in recent years the Society of Thoracic Surgeons continues to report more specific predictors and is updated annually to provide valuable risk data on CABG, valve, and combined procedures based on increasing volumes of cumulative data, making this perhaps the most robust of the risk indices.


   B. Functional status. For patients undergoing most general and cardiac surgical procedures, perhaps the simplest and single most useful risk index is the patient’s functional status, or exercise tolerance. In major noncardiac surgery, Girish and colleagues found the inability to climb two flights of stairs showed a positive predictive value of 82% for postoperative pulmonary or cardiac complications [13]. This is an easily measured and sensitive index of cardiovascular risk, which takes into account a wide range of specific cardiac and noncardiac factors.

   The level of exercise producing symptoms, as described classically by the New York Heart Association and Canadian Cardiovascular Society classifications, predicts the risk of both an ischemic event and operative mortality. During coronary revascularization procedures, operative mortality for patients with class IV symptoms is 1.4 times that of patients without preoperative congestive heart failure [14].

   C. Genomic contributions to cardiac risk assessment. Genetic variations are the known basis for more than 40 cardiovascular disorders. Some of these, including familial hypercholesteremia, hypertrophic cardiomyopathy, dilated cardiomyopathy, and “channelopathies” such as the long QT syndrome, are known as monogenetic disorders, caused by alterations in one gene. These usually follow traditional Mendelian inheritance patterns, and their genetic basis is relatively easy to identify. Genetic testing is able to identify these diseases in up to 90% of patients before they become symptomatic, allowing prophylactic treatment and early therapy. For example, genetic identification of the sub-type of long QT syndrome can determine an affected patient’s risk of dysrhythmias associated with exercise, benefit from β-blockers, or need for Implantable Cardioverter Defibrillator (ICD) implantation [15].

   Some of the areas of the greatest expansion of genomic medicine, however, are in its application to chronic diseases such as coronary artery and vascular disease. However, the causes of these disorders are multi-factorial, including environmental as well as genetic factors, and are at best due to complex interactions of many genes. Nevertheless, genetic information can be used to determine a patient’s susceptibility to disease, and this information can guide prophylactic therapy. Commercial tests are currently available for susceptibility to atrial fibrillation (AF) and MI. Genetic variants have been found which help to determine susceptibility to preoperative complications, including 4 which help to determine susceptibility to postoperative MI and ischemia. Similarly, genetic information may be used to determine variations in patient susceptibility to drugs, as for example a single allele variation can render patients much more susceptible to warfarin. Gene therapy may also target drug delivery to specific tissues [15].

Table 3.1 Multifactorial indices of cardiovascular risk for cardiac surgical procedures: summary of risk factors in recent multifactorial indices

Table 3.2 Cardiac anesthesia risk evaluation (CARE)

   D. Risk associated with surgical problems and procedures. The complexity of the surgical procedure itself may be the most important predictor of perioperative morbidity for many patients. Most, but not all, cardiac surgical procedures include the risks associated with cardiopulmonary bypass. Any procedure requiring cardiopulmonary bypass is associated with greater morbidity, caused by a systemic inflammatory response along with the risk of microemboli and hypoperfusion and most often involving the central nervous system, kidneys, lungs, and gastrointestinal tract. The extent of morbidity increases with the increased bypass duration.

   Procedures on multiple heart valves, or on both the aortic valve and coronary arteries, carry a statistical morbidity much higher than that for procedures involving only a single valve or CABG alone. The mortality rate over the last decade for each procedure, for patients in the Society of Thoracic Surgeons database, is approximately 2.3% for CABG, 3.4% for isolated valve procedures, and 6.8% for valve procedures along with CABG [3,14,16].

II. Preoperative medical management of cardiovascular disease

   A. Myocardial ischemia. In patients with known CAD, the most important risk factors that need to be assessed preoperatively are: (i) the amount of myocardium at risk; (ii) the ischemic threshold, or the heart rate at which ischemia occurs; (iii) the patient’s ventricular function or ejection fraction (EF); (iv) the stability of symptoms, because recent acceleration of angina may reflect a ruptured coronary plaque; and (v) adequacy of current medical therapy.

      1. Stable coronary syndrome (stable angina pectoris). Chronic stable angina most often results from obstruction to coronary artery blood flow by a fixed atherosclerotic coronary lesion in at least one of the large epicardial arteries. In the absence of such a lesion, however, the myocardium may be rendered ischemic by coronary artery spasm, vasculitis, trauma, or hypertrophy of the ventricular muscle, as occurs in aortic valve disease.

          Neither the location, duration, or severity of angina, nor the presence of diabetes or peripheral vascular disease (PVD), indicate the extent of myocardium at risk, or the anatomic location of the coronary artery lesions. Therefore, the clinician must depend on diagnostic studies, such as myocardial perfusion imaging (MPI), stress echocardiography, and cardiac catheterization to assist in establishing risk. Though some centers use cardiac computed tomography (CT) scanning for this purpose, and though it does have a high sensitivity for detecting coronary calcification and coronary artery disease, it currently still has a low specificity, so it cannot yet be recommended as a definitive test. In patients with chronic stable angina, a reproducible amount of exercise, with its associated increases in heart rate and blood pressure, often precipitates angina. This angina threshold, which can be determined on preoperative exercise testing, is an important guide to perioperative hemodynamic management. Stable angina often responds to medical therapy as well as to PCI. Patients are referred for CABG surgery when refractory to medical therapy and not candidates for PCI.

        a. Principles of the medical management of stable angina [17]

           (1) aspirin at 75 to 162 mg daily

           (2) β-blockade as initial therapy when not contraindicated

           (3) calcium antagonists or long-acting nitrates as second-line therapy, or as first-line therapy when beta blockade is contraindicated

           (4) use of ACE inhibitors indefinitely in patients with left ventricle (LV) EF <40%, diabetes, hypertension, or chronic renal failure

           (5) annual influenza vaccine

           (6) reducing risk by:

             (a) Lipid management—reduce low density lipoproteins to <100 mg/dL using diet, exercise, and statin therapy.

             (b) Blood pressure control—reduce to less than 140/90 or to less than 130/80 for patients with diabetes or kidney disease, for patients with coronary disease initially treating with β-blockers and ACE inhibitors.

             (c) Smoking cessation

             (d) Diabetes control

             (e) Weight loss

             (f) Diet and exercise

      2. Acute coronary syndrome (unstable angina pectoris). Sometimes called crescendo angina, or unstable coronary syndrome, this symptom complex usually presents as:

        a. Rest angina, within the first week of onset

        b. New onset angina markedly limiting activity, within 2 wks of onset

        c. Angina which is more frequent, of longer duration, or occurs with less exercise.

            These symptoms often indicate rapid growth, rupture, or embolus of an existing plaque. Patients in this category have a higher incidence of MI and sudden death, and increased incidence of left main occlusion. The clinical factors important in determining the risk of MI or death in patients with unstable angina are shown in Table 3.3.

        d. Medical management for acute coronary syndrome. Diagnostic and revascularization procedures are the central parts of the management for most patients with acute coronary syndrome. However, they are often accompanied or preceded by medical therapy. The medical management of unstable angina or of a non-ST segment elevation MI has two parts: (i) anti-ischemic therapy and (ii) antiplatelet and anticoagulant therapy. Medical anti-ischemic therapy depends largely on the presence or absence of ongoing ischemia and must be accompanied by an aggressive approach to secondary prevention or risk factor modification (Table 3.4 and Table 3.5).

      3. Myocardial ischemia without angina may be manifested by fatigue, rapid onset of pulmonary edema, cardiac arrhythmias, syncope, or an “anginal equivalent,” most often characterized as indigestion or jaw pain. Silent ischemia is more common in the elderly and diabetic patients, with 15% to 35% of all MIs occurring as silent events, documented only on routine electrocardiogram (ECG). Whether related to coexisting disease or delayed therapy, silent ischemia has been associated with an unfavorable prognosis.

      4. Prior MI interval between prior infarction and surgery.

          In the non-cardiac surgical population, the occurrence of an MI within the 30 d before surgery is a significant preoperative risk factor [10]. Bernstein [6] assigns additional risk to an MI occurring 48 hrs before surgery and Eagle et al. [18] conclude that CABG has increased risk in patients with unstable angina, early postinfarction angina (within 2 days of a non-ST-Elevation Myocardial Infarction (non-STEMI) and during an acute MI), and that risk may be reduced by delaying CABG for 3 to 7 days after MI in stable patients. Coronary revascularization procedures, however, offer improved survival in patients with unstable angina and LV dysfunction.

Table 3.3 Risk factors for death or MI in patients with unstable angina

   B. Congestive heart failure

      1. Clinical assessment and medical management of heart failure. Ventricular dysfunction can occur almost immediately in association with an ischemic event. If no infarction occurs and the myocardium is reperfused, the ventricle recovers function quickly. Short episodes of ischemia followed by reperfusion may actually precondition the heart, so when it is exposed to more severe ischemia, the size and severity of MI is reduced. A MI may be associated with “stunned” myocardium, which recovers function within days to weeks, or “hibernating” myocardium, which may recover months after infarction and revascularization. Ventricular dysfunction and heart failure have been classified into four stages, A through D, based on cardiac structural changes and symptoms of heart failure. Management depends on the stage of the disease. ACE inhibitors and angiotensin II receptor blockers are usually used as first-line therapy, with the addition of β-blockers, aldosterone antagonists, diuretics, and implanted devices for more severely affected patients (Fig. 3.1).

      2. Perioperative morbidity. Evidence of congestive heart failure or ventricular dysfunction preoperatively is associated with an increased operative mortality. Recent series summarized in Table 3.1 show a 1.5- to 2.5-fold greater risk of postoperative morbidity or mortality in patients with preoperative congestive heart failure, and a 1.4- to 12-fold greater risk in patients with preoperative cardiogenic shock.

          In patients undergoing aortic valve replacement (AVR) for critical aortic stenosis and depressed EF, a cardiothoracic ratio of 0.6 is possibly the most important predictor of operative mortality, increasing the risk in some series more than 10-fold.

Table 3.4 Medical therapy for unstable angina: anti-ischemic therapy

Table 3.5 Medical therapy for unstable angina and non-ST elevation MI: antiplatelet and anticoagulation therapy

Figure 3.1 Functional classification and stages in the development of heart failure, and medical management of each stage. ACEI, angiotensin-converting enzyme inhibitor; ARB, angiotensin II receptor blocker; EF, ejection fraction; FHx CM, family history of cardiomyopathy; HF, heart failure; LV, left ventricular; LVH, left ventricular hypertrophy; and MI, myocardial infarction. [From Hunt SA, Abraham WT, Marshall HC, et al. 2009 Focused update incorporated into the ACC/AHA 2005 guideline update for the diagnosis and management of heart failure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing committee to update the 2001 guidelines for the evaluation and management of heart failure). Circulation2009;119:e391–e479]

   C. Dysrhythmias

      1. Incidence. Cardiac dysrhythmias are common in patients presenting for cardiac surgery, and become increasingly common with age after 50. In the perioperative period, abnormal rhythms occur in more than 75% of patients. However, those dysrhythmias are life-threatening in less than 1%.

      2. Supraventricular tachycardia (SVT). SVTs appear most often in the preoperative history as palpitations or near-syncope. AF and flutter, the most common SVTs, increase in frequency with age and in association with organic heart disease. Preoperative patients with SVT who are hemodynamically stable are usually managed acutely with vagal maneuvers, adenosine, verapamil, or diltiazem to reduce heart rate and potentially convert the SVT back to sinus rhythm. Those with AF are in addition managed with anticoagulation to reduce stroke risk. However, in the last two decades, either surgical or catheter-based ablation have become more common, especially in patients unresponsive to medical therapy or in whom there may be structural abnormalities.

      3. Ablation therapy

        Catheter ablation using radiofrequency (RF) energy was first used in 1982. Medication can often control atrioventricular (AV) nodal reentrant tachycardia, However, when medications are ineffective, RF ablation can be performed. This procedure has a 97% success rate, 5% recurrence rate during the patient’s lifetime, and causes heart block requiring pacer therapy in 0.5% to 1% of patients in which it is used [19].

          AF is the most frequent supraventricular arrhythmia. It can be caused by multiple reentrant circuits and also by a single focus in the SVC or pulmonary veins. Antiarrhythmic drugs can maintain sinus rhythm in one-half to two-third of patients with AF but may reduce the quality of life, decrease left ventricular function, and increase the risk of embolic complications.

          The Maze procedure is a surgical procedure which disrupts the re-entrant pathways or ablates arrhythmogenic foci in the atria, often by isolating the ostia of the pulmonary veins. Thereby it converts the fibrillation to sinus rhythm, reducing the need for anticoagulation. However, this procedure is not always successful, and therefore a second type of procedure ablates the AV node, isolating the fibrillating atria from the ventricles, without attempting to prevent the AF itself. This procedure requires a permanent pacemaker to drive the ventricles, as well as ongoing anticoagulation to prevent thrombosis in the fibrillating atria.

          The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) investigated the relative benefits of simple AF rate control versus conversion to sinus rhythm in patients older than age 65 [20]. Though the two treatments led to no difference in major bleeding, death, stroke, or quality of life, antiarrhythmic therapy and catheter ablation were recommended in symptomatic individuals in whom the arrhythmia interferes with their regular activities. A worldwide AF ablation survey reported 4550 of 8745 patients (52%) in sinus rhythm after ablation alone. With drug therapy, they reported a 75.9% success rate [21].

      4. Ventricular arrhythmias and VT. Ventricular dysrhythmias have been classified according to clinical presentation (stable or unstable), type of rhythm (sustained or nonsustained VT, bundle-branch re-entrant or bidirectional VT, Torsades de pointes, ventricular flutter or fibrillation), or associated disease entity. Ventricular arrhythmias may lead directly to ventricular fibrillation and sudden cardiac death, especially if they occur in the setting of acute or recent infarction. However, isolated asymptomatic ventricular arrhythmias, even nonsustained VT, have not been associated with complications following noncardiac surgery. Patients with preoperative ventricular arrhythmias associated with left ventricular dysfunction and an EF < 30% to 35% are often managed with the prophylactic implantation of an ICD. Those not controlled with or not candidates for ICD therapy are managed medically with β-blockers as the first-line therapy. Amiodarone is the second-line drug used to prevent sudden cardiac death, with studies showing some survival benefit, and sotalol can also be effective though with greater proarrhythmic effects [22].


      5. Bradycardia. Anesthetics frequently affect sinus node automaticity but rarely cause complete heart block. Asymptomatic patients with ECG-documented AV conduction disease (PR prolongation or single or bifascicular bundle branch block) rarely require temporary pacing perioperatively. However, symptomatic patients, or patients with Mobitz II or complete heart block, require preoperative evaluation for permanent pacing. Patients with a recent MI or with both first-degree AV block and bundle branch block may need temporary transvenous or transcutaneous pacing perioperatively (See Chapter 17—“Rhythm Management Devices”).

          Patients with left bundle branch block in whom a Swan-Ganz catheter is being placed may need availability of a transcutaneous pacemaker because of the risk of inducing right bundle branch block, and thus complete heart block, during passage of the pulmonary artery catheter. Patients with a left bundle branch block and right CAD may be at particular risk during the passage of a Swan-Ganz catheter.


          Patients with an indwelling cardiac pacemaker or ICD need to have their device identified and evaluated preoperatively. Special precautions need to be considered, as outlined in Chapter 17, to prevent untoward effects of electromagnetic interference in the operating room.

   D. Hypertension

Systemic hypertension is one of the most common diseases of adulthood and is perhaps the most treatable cause of cardiovascular morbidity, including MI, stroke, PVD, renal failure, and heart failure. The contribution of hypertension to perioperative morbidity and the implications for anesthetic management depend on (i) blood pressure level, both with stress and at rest; (ii) the etiology of hypertension; (iii) pre-existing complications of hypertension; and (iv) physiologic changes due to drug therapy.

      1. Blood pressure level. Data summarized in the JNC VII report in 2003 indicate that cardiovascular risk begins to increase at blood pressures above 115/75 and doubles with each increment of 20/10. Patients with blood pressures of 120–139/80–89 are considered prehypertensive and require drug therapy if they have associated diabetes or renal disease. Patients with blood pressures of 140–159/90–99 are considered hypertensive and all require chronic drug therapy. Those with blood pressures greater than 160/100, classified as stage 2 hypertensive, usually require combination drug therapy. Further, for patients older than 50 yrs, systolic blood pressure >140 is a much more important cardiovascular risk factor than diastolic blood pressure [23].

          In contrast to the usual emphasis on the resting, unstimulated blood pressure in determining chronic medical management, preoperatively the patient’s blood pressure under stress, as in the preoperative clinic or holding area, may be a better predictor of their perioperative morbidity. Intraoperative cardiac morbidity in the form of dysrhythmias and ischemic ECG changes may be more frequent in Stage 3 hypertensive patients with awake systolic blood pressures greater than 180 mm Hg and diastolic blood pressures of greater than 110 mm Hg, and this morbidity may be reduced by preoperative treatment. In these patients the benefits of improving hypertensive control preoperatively should be weighed against the risks of delaying surgery. Blood pressure lower than 180/110 has not been found to be an important predictor of increased perioperative cardiac risk, but it may be a marker for chronic cardiovascular disease [10].


      2. Etiology. The most common “primary” or “essential” hypertension is likely caused by a combination of multiple genetic and environmental factors, with the genetic contribution, at least, being irreversible. However, it is important preoperatively to exclude the 5% to 15% of patients with treatable causes of secondary hypertension, especially patients shown in Table 3.6. Common causes of secondary hypertension are usually renal, endocrine, or drug related, which account for an additional 5% to 10% of hypertensive patients. Other rare disorders are found in less than 1% of patients (Table 3.7). A laboratory investigation of secondary hypertension, when indicated, should include urinalysis, creatinine, glucose, electrolytes, calcium, EKG, and chest films. More extensive testing is usually not indicated unless blood pressure cannot be controlled or a high clinical suspicion exists [23]. Pheochromocytoma, although very rare, is particularly important because of its potential morbidity in association with anesthesia. Therefore, it should be ruled out preoperatively in patients with headache, labile or paroxysmal hypertension, abnormal pallor, or perspiration, even if delay of surgery is required.

Table 3.6 Risk factors for secondary hypertension

Table 3.7 Causes of hypertension

      3. Sequelae of hypertension. The hypertensive state can lead to sequelae most evident in the heart, central nervous system, and kidney. In particular, patients with established hypertension may exhibit (i) LV hypertrophy leading to decreased ventricular compliance; (ii) neurologic symptoms, such as headache, dizziness, tinnitus, and blurred vision that may progress to cerebral infarction; and (iii) renal vascular lesions leading to proteinuria, hematuria, and decreased glomerular filtration progressing to renal failure.

      4. Antihypertensive therapy. Today antihypertensive medications are the most prescribed class of medications, and more than 75 individual or combination drugs are prescribed. The primary objective of antihypertensive therapy is to reduce cardiovascular morbidity by lowering the blood pressure. However, specific classes of antihypertensive agents are effective in preventing end organ damage, especially to the heart and the kidney, beyond that directly associated with lowering the blood pressure. The recommended antihypertensive drug classes for patients with specific comorbid conditions are shown in Table 3.8[23]. The properties of specific medications are discussed in Chapter 2.

   E. Cerebrovascular disease

      1. The association of preoperative cerebrovascular disease with increased perio-perative neurologic dysfunction. CNS dysfunction of at least some degree is common after cardiopulmonary bypass with temporary postoperative neurocognitive defects occurring in up to 80% of patients and stroke in 1% to 5% [24]. Arrowsmith, et al. found that aortic atherosclerosis is associated with the highest risk of adverse neurologic events (odds ratio 4.52) and that a history of neurologic disease ranked second, with an odds ratio of 3.19 [25]. Patients with a preoperative stroke are more likely to have a perioperative stroke. Even in the absence of a prior cerebral ischemic event, the presence of carotid stenosis increases the risk of postoperative stroke from approximately 2% in patients without carotid stenosis to 10% with stenosis of greater than 50%, and to 11% to 19% with stenosis of greater than 80% [26].

Table 3.8 Antihypertensive therapy for patients with other systemic disease


      2. Genetic factors. Genetic factors may modify the risk or severity of postoperative CNS injury. Genes related to thrombotic factors and inflammatory factors such as platelet receptors, C-reactive protein, and interleukin-6, have been associated with the risk of postoperative cognitive dysfunction.

      3. Effect of the surgical procedure. Cardiopulmonary bypass may increase the risk of postoperative cognitive dysfunction, but neurologic deficits are still seen following off pump coronary artery bypass surgery, likely because of effects such as blood pressure lability, low cardiac output, the systemic inflammatory reaction to the procedure, or manipulation of the ascending thoracic aorta.

          As may be expected, several authors have shown increased postoperative cerebral dysfunction following open aortic or mitral valve procedures compared to CABG. However, in these series, the duration of cardiopulmonary bypass was also longer for the valve procedures, making it difficult to establish a causal relationship. Even though it is apparent that carotid artery stenosis represents a risk factor for perioperative stroke, it is not nearly as clear that simultaneous carotid endarterectomy reduces this risk. Therefore, recent texts recommend that combined carotid endarterectomy and CABG not usually be undertaken. Rather, at the present time epiaortic scanning to modify the surgical technique during the cardiac procedure, and possibly neurophysiologic monitoring, may offer more benefit [27].

III. Noninvasive cardiac imaging

   A. Echocardiography. Transthoracic echocardiography provides specific preoperative assessment of several types of cardiac abnormalities. First, two dimensional (2D) and Doppler echocardiography together provide quantitative assessment of the severity of valvular stenosis or insufficiency (see Chapter 12) and of pulmonary hypertension. Second, assessment of regional wall motion provides a more sensitive and specific assessment of the existence and extent of MI than a surface EKG. Third, 2D echocardiography provides a quantitative assessment of global ventricular function, or ejection fraction (EF). Fourth, echocardiography can detect even small pericardial effusions. Fifth, echocardiographs can detect anatomic cardiac abnormalities, from atrial septal defects (ASD) and ventricular septal defects (VSD) to aneurysms and mural thrombi.

   Perioperative transthoracic echocardiography predicts postoperative cardiac events in noncardiac surgical patients at increased clinical cardiac risk. Decreased preoperative systolic dysfunction on echo has been associated with postoperative MI, pulmonary edema, and “major cardiac events,” such as ventricular fibrillation, cardiac arrest, or complete heart block. LV hypertrophy, mitral regurgitation, and increased aortic valve gradient on preoperative echo also appear to predict postoperative “major cardiac events.”

   B. Preoperative testing for myocardial ischemia

      1. Exercise tolerance testing. The exercise tolerance test (ETT) is often used as a simple and inexpensive initial test to evaluate chest pain of unknown etiology. It is also used preoperatively to determine functional capacity and identify significant ischemia or dysrhythmias for prognostic stratification preoperatively. ETT is rarely useful as a screening test in asymptomatic patients. To better address the prognostic value of the ETT, the Duke risk score was developed [28]. This risk score equals the exercise time in minutes, minus five times the extent of the ST segment depression in millimeters, minus four times the level of angina with exercise (0—no angina, 1—typical angina, 2—typical angina requiring stopping the test). The score typically ranges from –25 to +15. These values correspond to low-risk (with a score of +5), moderate-risk (with scores ranging from –10 to +4), and high-risk (with a score of <–11) categories.

        a. Limitations of ETT

           (1) Inability to exercise because of systemic disease, particularly PVD.

           (2) Abnormal resting ECG precluding ST segment analysis (left bundle branch block, LV hypertrophy, digoxin therapy).

           (3) β-blocker therapy that prevents the patient from achieving 85% of his or her maximum permissible heart rate.

      2. Stress echocardiography. Stress echocardiography can use exercise stress or pharmacologic stress, with dobutamine, to increase myocardial work. Abnormally contracting myocardial segments seen on stress echocardiography are classified as either ischemic, if their reduced contraction pattern is in response to stress, or infarcted, if their contractility remains consistently depressed before, during, and after stress.

          Sixteen recent studies evaluated in the 2007 ACC/AHA Guidelines for Perioperation Cardiovascular Evaluation showed that 0% to 33% of vascular patients who had a positive preoperative Dobutamine Stress Echocardiogram (DSE) subsequently suffered a post operative MI or death. The negative predictive value was much higher—93% to 100% [10]. Wall motion abnormalities at low workloads were especially important predictors of short- and long-term outcomes. DSE has indications similar to pharmacologic perfusion imaging with comparable sensitivity, but possibly increased specificity.

          For patients with poor acoustic windows due to body habitus or severe lung disease, myocardial contrast agents are now available to improve imaging. Still, for some patients, a difficult echocardiographic window or global poor ventricular function may preclude its use. Further, this test cannot be used for those patients in whom a recent MI, an intracranial or abdominal aneurysm, or other vascular malformation would make tachycardia or hypertension risky.

      3. Radionuclide imaging. Radionuclide stress imaging is used to assess the perfusion and the viability of areas of myocardium. This technique cannot provide an anatomic diagnosis of a cardiac lesion. It is a more sensitive and specific test than ETT and can provide an assessment of global LV function as well. MPI is a nuclear technique employing intravenous radioisotopes, either thallium-201 or the cardiac-specific technetium-99 perfusion agents, sestamibi (Cardiolite), or tetrofosmin (Myoview), as an indicator of the presence or absence of CAD.

          Exercise stress or pharmacologic stress is necessary to increase coronary blood flow for the test. Pharmacologic vasodilators are preferable but contraindicated in patients with severe bronchospastic lung disease, in which case dobutamine may be used. The available pharmocologic vasodilators—adenosine (Adenoscan), dipyridamole (Persantine), and regadenoson (Lexiscan)—are used to produce maximal coronary vasodilation of approximately four to five times resting values. Vessels with fixed coronary stenoses will not dilate, allowing less isotope to reach the myocardium. Myocardium underperfused by these vessels will show up as a “defect” on stress scans when compared to surrounding myocardium supplied by nonobstructed coronaries. When compared to the images acquired at rest, any defects still present—fixed or persistent defects—are suggestive of nonviable or infarcted myocardium. Defects present on stress and not at rest, termed reversible defects, suggest viable myocardium at risk for ischemia when stressed.

          A perfusion scan may be performed in three different ways. When thallium is chosen, only a single injection is required because the isotope redistributes; however, a repeat image should be taken 4 hrs after the stress images are taken. With the technetium agents, particularly best for larger patients due to the higher energy (KeV), separate rest and stress injections are required because no redistribution is seen. Finally, dual isotopes studies utilizing thallium for the initial rest image and technetium for the stress image allows for the fastest patient through put.

          The technique used to acquire these images is single photon-emission computed tomography (SPECT). In the studies of noncardiac surgical patients reviewed by the ACC/AHA Task Force on Perioperative Cardiovascular Evaluation, reversible defects on nuclear perfusion scanning identified 2% to 20% of patients suffering postoperative MI or cardiac death. The negative predictive value of a normal scan is much better, at approximately 99%. Fixed defects did not usually predict perioperative cardiac events. The sensitivity and specificity of nuclear perfusion imaging is similar for pharmacologic and stress-based techniques [10]. The predictive value of the test can be improved by using it in high-risk sub-groups. Selective use of pharmacologic perfusion imaging in only patients who have at least one of two clinical risk factors for ischemic disease (age >70 yrs and congestive heart failure) can maximize the usefulness of this procedure in predicting cardiac outcome in patients undergoing noncardiac surgery of all types.

          Contraindications to pharmacologic stress with dipyridamole, adenosine or regadenoson are:


     • unstable angina or MI within 48 hrs

     • severe primary bronchospasm

     • methylxanthine ingestion within 24 hrs

     • allergy to dipyridamole or aminophylline

     • For adenosine only, first-degree heart block (PR interval >0.28 seconds) and recent oral dipyridamole ingestion (<24 hrs ago).

          Pharmacologic vasodilators should be used in patients who cannot exercise, or have a medical condition, such as a cerebral aneurysm, which would contraindicate exercise. Pharmacologic stress testing with vasodilators, such as adenosine or dipyridamole, is also preferable to exercise or dobutamine in patients with left bundle branch block, because of spurious septal changes with exercise or catecholamines, which lead to false positive tests.

      4. Positron emission tomography (PET) scan. PET scanning techniques use different radioisotopes than SPECT imaging. These isotopes decay with a higher energy photon with a shorter half life and can assess both regional myocardial blood flow and myocardial metabolism on a real-time basis. PET scanning techniques can be combined with CT and magnetic resonance imaging (MRI) to provide PET metabolic and anatomic information simultaneously.

      5. Magnetic resonance imaging (MRI). MRI has been used for some time to provide both high resolution and three-dimensional imaging of cardiac structures. It is now becoming important in perfusion imaging, atherosclerosis imaging, and coronary artery imaging. With the development of dedicated cardiovascular MRI scanning, molecular imaging techniques and biochemical markers are providing the capacity for MRI diagnosis of cardiac function. Changes in molecular composition of the myocardium can change its magnetic moment and MRI signal, allowing MRI to detect lipid accumulation, edema, fibrosis, rate of phosphate turnover, and intracellular pH in ischemic areas. Finally, MRI imaging can be gated to the cardiac cycle, allowing rapid and accurate assessment of myocardial function. Gated images are used to detect regional myocardial abnormalities that may be caused by ischemia, infarction, stunning, hibernation, and postinfarct remodeling. MRI is the diagnostic technique of choice for arrhythmogenic right ventricular (RV) dysplagia and can differentiate myocardial infiltration and diastolic dysfunction associated with sarcoidosis, hemochromatosis, amyloidosis, and endomyocardial fibrosis. Contrast-enhanced MRI has a higher sensitivity and specificity than either CT scan or TEE in aortic dissection. Dobutamine stress MRI is an accurate and rapid test for myocardial ischemia, which may eventually replace dobutamine echocardiography.

          MRI can be used to diagnose CAD involving the native major epicardial arteries with an accuracy of approximately 87% and is even better for assessing saphenous vein and internal mammary artery graft patency. However, it is still not commonly used clinically for this purpose.

      6. Computed tomography. Since its introduction into clinical practice in 1973, CT has undergone significant advances. CT for calcium scoring has been utilized clinically to estimate cardiac risk but is not effective for defining atherosclerotic disease. With the development of a higher temporal resolution scan, in conjunction with contrast injection, coronary imaging is now possible. As these imaging techniques advance in the cardiology arena, they can be used for imaging the pericardium, cardiac chambers, and great vessels. However, imaging protocols require aggressive β-blockade to achieve heart rates of 60 bpm or less in order to decrease image blurring and improve resolution.

          Though more widely applied in recent years, less extensive clinical expertise and prognostic data preclude recommending this technique as a substitute for other more established diagnostic techniques at this time.

IV. Cardiac catheterization

   A. Overview. Cardiac catheterization still is considered the gold standard for diagnosis of cardiac pathology before most open heart operations and for definition of lesions of the coronary vessels. More than 95% of all patients undergoing open heart operations have had catheterization prior to the procedure. The remaining 5% are assessed only by noninvasive techniques, such as echocardiography and Doppler flow studies. They have pathologic findings, such as an ASD or VSD, which are adequately defined by noninvasive means.

   As an invasive procedure, serious complications occur in approximately in 0.1% of patients and include stroke, heart attack, and death. Significant access site complications occur in approximately 0.5%.

   If only coronary anatomy is to be delineated, often only a systemic-arterial or left-sided catheterization will be performed. However, if any degree of LV dysfunction, valvular abnormality, pulmonary disease, or impaired RV function exists clinically, a right-sided (Swan-Ganz) catheterization will also be performed. A range of normal hemodynamic values obtained from right- and left-sided catheterization is included in Table 3.9.

   Interpretation of catheterization data emphasizes the following areas.

   B. Assessment of coronary anatomy

      1. Procedure. Radiopaque contrast is injected through a catheter placed at the coronary ostia to delineate the anatomy of both the right and left coronary arteries. Multiple views are important to define branch lesions, decrease artifacts at points of tortuosity or vessel overlap, and determine more clearly the degree of stenosis, particularly in eccentric lesions. Two common projections of the coronary arteries are the right anterior oblique (RAO) and the left anterior oblique (LAO) views (Fig. 3.2).

      2. Interpretation. The degree of vessel stenosis generally is assessed by the percent reduction in diameter of the vessel, which in turn correlates with the reduction in cross-sectional area of the vessel at the point of narrowing. Lesions that reduce vessel diameter by greater than 50%, reducing the cross-sectional area by greater than 70%, are considered significant. Lesions are also characterized as either focal or segmental. There is a great deal of inter-observer variability in interpretation with particular concern regarding intermediate lesions (50% to 70%) and their physiologic significance. Adjunct imaging techniques include fractional flow reserve (FFR) and intravascular ultrasound (IVUS) that may assist in defining the need for revascularization of these vessels.

Table 3.9 Normal hemodynamic values obtained at cardiac catheterization

Figure 3.2 Representation of coronary anatomy relative to the interventricular and AV valve planes. Coronary branches are L Main, left main; LAD, left anterior descending; D, diagonal; S, septal; CX, circumflex; OM, obtuse marginal; RCA, right coronary; CB, conus branch; SN, sinus node; AcM, acute marginal; PD, posterior descending; PL, posterolateral left ventricular. RV, right ventricle. (Reproduced from Baim DS, Grossman W. Coronary angiography. In: Grossman W, ed. Cardiac catheterization and angiography. 3rd ed. Philadelphia: Lea & Febiger, 1986:185, with permission.)

   C. Assessment of left ventricular function. Both global and regional measures of ventricular function can be obtained from catheterization data.

      1. Global ventricular measurements

        a. Left ventricular end-diastolic pressure (LVEDP). An elevated value above 15 mm Hg usually indicates some degree of ventricular dysfunction. LVEDP is an index that may reflect either systolic or diastolic dysfunction and is acutely affected by preload and afterload. Without examining other indices of function, an isolated measurement of elevated LVEDP simply indicates that something is abnormal. Associated with a normal LV contractile pattern and cardiac output, an elevated LVEDP measurement may indicate a decrease in left ventricular compliance.

        b. Left ventricular EF

           (1) Calculation. EF is defined as the volume of blood ejected (stroke volume (SV)) per beat divided by the volume in the LV before ejection The SV is equal to the EDV minus the end-systolic volume (ESV). The equation for EF determination is therefore:

           (2) Mitral regurgitation. An EF of greater than 50% is normal in the presence of normal valvular function. However, in the presence of significant mitral regurgitation, an EF of 50% to 55% suggests moderate LV dysfunction, because part of the volume is ejected backward into a low-resistance pathway (i.e., into the left atrium).

      2. Regional assessment of ventricular function. LV contraction observed during ventri-culography provides a qualitative assessment of overall ventricular function but is not as specific as the calculated EF. Routine ventriculography is less commonly performed when concerns for contrast volume, patient instability or prior assessment of function are present.

          Qualitative regional differences in contraction may be evident. For examination, the heart is divided into segments. The anterior, posterior, apical, basal, inferior (diaphragmatic), and septal regions of the LV are examined (Figs. 3.3 and 3.4). Motion of each one of these particular regions is defined as normal, hypokinetic (decreased inward motion), akinetic (no motion), or dyskinetic (outward paradoxical motion) in relation to the other normally contracting segments.

Figure 3.3 Terminology for left ventricular segments 1–5 analyzed from right anterior oblique ventriculogram. LV, left ventricle; LA, left atrium. (Reproduced from CASS Principal Investigators and Associates. National Heart, Lung, and Blood Institute Coronary Artery Surgery Study [Part II]. Circulation 1981;63[Suppl.]:1–14, Figure 2, with permission.)

Figure 3.4 Terminology for left ventricular segments 6–10 analyzed from left anterior oblique ventriculogram. LV, left ventricle; LA, left atrium. (Reproduced from CASS Principal Investigators and Associates. National Heart, Lung, and Blood Institute Coronary Artery Surgery Study [Part II]. Circulation 1981;63[Suppl.]:1–14, Figure 3, with permission.)

          Regional wall motion abnormalities are usually secondary to prior infarction or acute ischemia. However, very infrequently myocarditis as well as rare infiltrative processes by myocardial tumors may lead to regional wall motion abnormalities.

   D. Assessment of valvular function. This section will be limited to a brief discussion of the methods utilized to study lesions of the aortic and mitral valves. The specific hemodynamic patterns of acute and chronic valvular disease will be discussed in Chapter 12.

      1. Regurgitant lesions

        a. Qualitative assessment. A relative scale of 1+ to 4+ (4+ being the most severe) is used to quantify the severity of valvular incompetence during the injection of dye. Visual inspection is utilized to determine the intensity and rapidity of washout of dye from the LV after aortic root injection (aortic regurgitation) or from the left atrium after ventricular injection (mitral regurgitation).

        b. Pathologic V waves. In patients with mitral regurgitation, the pulmonary capillary wedge trace may manifest giant V waves. Normal or physiologic V waves are seen in the left atrium at the end of systole and are secondary to filling from the pulmonary veins against a closed mitral valve. With valvular incompetence, the regurgitant wave into the left atrium is superimposed on a physiologic V wave, producing a giant V wave (Fig. 3.5).

      2. Stenotic lesions. The severity of valvular stenosis can be determined only by knowing the size of the pressure drop across the stenotic valve and the flow across the stenosis during either systolic ejection or diastolic filling. One cannot uniformly assess the severity of stenosis solely by examining the pressure gradient across the valve.

          Gorlin and Gorlin [29] described an equation for determining valve area based on these two factors in the American Heart Journal in 1951. A simplified version of this equation is:

          With the peak pressure gradient and cardiac output given on the catheterization report, a quick estimate of either aortic or mitral valve area can be made.

          When examining combined regurgitant and stenotic lesions of the same valve, the total or angiographic cardiac output must be used in the calculation; otherwise, the severity of stenosis will be overestimated. Values for normal and abnormal valve areas are discussed in Chapter 12.

          Remember that catheterization data represent only one point in time, and medical management may have changed the hemodynamic pattern and catheterization results at the time of cardiac operation.

Left ventricular (LV) and pulmonary capillary wedge (PC) pressure tracings taken in a patient with ruptured chordae tendineae and acute mitral insufficiency. The giant V wave results from regurgitation of blood into a relatively small and noncompliant left atrium; ECG illustrates the timing of the PC V wave, whose peak follows ventricular repolarization, as manifest by the T wave of the ECG. (Reproduced from Grossman W. Profiles in valvular heart disease. In Grossman W, Baim DS, eds. Cardiac Catheterization, Angiography, and Intervention. 4th ed. Philadelphia: Lea & Febiger, 1991:564, with permission.)

V. Interventional Cardiac Catheterization

   A. Percutaneous coronary intervention (PCI). In 1977, Andreas Gruentzig brought therapeutic options to the invasive cardiology practice with the first percutaneous transluminal coronary angioplasty (PTCA). Multiple technologies have advanced since the initial balloon dilation. Current technology has evolved to include niche devices including rotational coronary atherectomy, various thrombectomy techniques, distal protection devices for saphenous vein graphs, and coronary stents [30].

   However, post-PCI re-stenosis, a recurrent blockage resulting from a local vascular response to injury, occurs in one-third of balloon dilations and limits their effectiveness. Intracoronary stents were developed to provide local stabilization for PCI-induced coronary dissection and to prevent re-stenosis. Their wide-spread use has significantly reduced the need for emergent coronary bypass surgery. The original BMS reduced restenosis rates significantly, while DES, covered with polymer-based anti-inflammatory medications, have reduced re-stenosis rates an additional 46–55% [31].

   The need for emergency coronary artery bypass graft surgery (CABG) has dramatically decreased with the use of coronary artery stents. Emergency CABG in patients undergoing PCI decreased from 2.9% before the use of stents to 0.3% with stents [32]. In 2009 the National Cardiovascular Data Registry (NCDR) reported the rate of emergency CABG following PCI was 0.4% [33].

   Several studies have reported on the frequency of procedure-related indications for emergent CABG following PCI. These include: dissection (27%), acute vessel closure (16%), perforation (8%), and failure to cross the lesion (8%). Three-vessel disease was also present in 40% of patients requiring emergency CABG [34]. The strongest predictors of the need for emergency CABG in several studies, however, are cardiogenic shock (OR = 11.4), acute MI or emergent PCI (OR = 3.2–3.8), multivessel or three-vessel disease (OR = 2.3–2.4), and type C lesion (OR = 2.6) [34]). In-hospital mortality for emergency CABG after PCI ranges from 7.8% to 14%.

   Though a large proportion of patients come for surgery with a history of PCI at some time in the past, it is now well established that PCI is not beneficial when used solely as a means to prepare a patient with coronary artery disease for surgery.


   B. Preoperative management of patients with prior interventional procedures

      1. Post-coronary stent anti-platelet therapy and stent thrombosis

        a. Coronary artery stent thrombosis

           Coronary artery stents are effective in preventing re-stenosis, but as foreign bodies they increase the long term, and perhaps even permanent, risk of coronary artery thrombosis. Metal stents are associated with the greatest inflammatory response, in the first 4 to 6 weeks, which then leads to re-epithelialization and a decrease in the risk of subsequent thrombosis after approximately 6 weeks. In contrast, DES are designed to inhibit inflammation and so these stents remain exposed for a much longer period of time, and so are associated with a much longer risk of stent thrombosis, extending at least to, and perhaps much longer than, 1 year. Unfortunately, there is no reliable way to determine when endothelialization actually occurs.

            Because thrombosis occurs quickly, in comparison to re-stenosis, it is associated with a very high risk (greater than 50% in some series) of MI and death. Therefore, antiplatelet therapy is required to reduce the risk of thrombosis. Anti-platelet therapy may be particularly useful in the perioperative period, with its associated thrombotic risk.

        b. Anti-platelet agents

          Aspirin and clopidogrel have been the mainstays of anti-platelet therapy. Since they work by different mechanisms, they have at least an additive, or perhaps super-additive effect. Ticlopidine is approximately as effective as clopidogrel in reducing the risk of thrombosis, but does have increased side effects. More recently, prasugrel has been introduced and cangrelor is an investigational drug, which may provide new therapeutic options preoperatively. Table 3.10 compares the properties of these four agents.

            Prasugrel has been found to be somewhat more effective than clopidogrel at reducing the risk of stent thrombosis, with its associated MIs and death. So, it may be useful for patients at extremely high risk of stent thrombosis. Cangrelor, appears to have a similar efficacy and a much more rapid onset and shorter duration, because of its reversible binding to receptors. Therefore, it is being studied as a possible purging agent, specifically used in patients with coronary artery stents in preparation for surgical procedures.

Table 3.10 Anti-platelet agents commonly used to prevent coronary stent thrombosis

Table 3.11 Risk factors for coronary stent thrombosis

        c. Prevention of coronary artery stent thrombosis

          Continuous treatment with the combination of aspirin and adenosine diphosphate (ADP) antagonist after PCI reduces major adverse cardiac events (MACE). On the basis of randomized clinical trials, aspirin 162 to 325 mg daily should be given for at least 1 month after PCI, followed by daily long-term use of aspirin indefinitely at a dose of 81 to 162 mg. In patients for whom there is concern about bleeding, the lowest dose of 81 mg can be used.

            Likewise, P2Y12 inhibitors (thienopyridines) should be given for a minimum of 1 month after BMS, as the second part of dual anti-platelet therapy (DAPT), with a minimum of 2 weeks for patients at significant increased risk of bleeding, and for 12 months after DES in all patients who are not at high risk of bleeding. In the US, there are currently four approved DES: sirolimus-eluting stents (SES), paclitaxel-eluting stents (PES), zotarolimus-eluting stents (ZES), and everolimus-eluting stents (EES). Each of these stents are presumed to be associated with delayed healing and a longer period of risk for thrombosis compared with BMS, and require longer duration of DAPT. Current guidelines recommend at least 12 months of DAPT following any DES in order to avoid late (after 30 days) thrombosis.

            A growing number of cardiologists, however, recommend extending DAPT beyond 1 year based on observational data analysis, and randomized trials to determine whether longer DAPT reduces stent thrombosis risk are in progress. Late stent thrombosis risk, after 1 year, is likely higher in DES than BMS and has been observed at a rate of 0.2% to 0.4% per year. The greatest risk of stent thrombosis is within the first year regardless of stent type and ranges from 0.7% to 3% depending on patient and lesion complexity [35].

            Risk factors for both early and late stent thrombosis are shown in Table 3.11. In addition, of course, any subsequent surgery would result in increased thrombotic risk in the perioperative period.

        d. Perioperative anti-platelet therapy in patients with coronary artery stents

          According to current recommendations, elective surgery requiring interruption of DAPT should not be scheduled within 1 month of BMS placement or within 12 months of DES placement. Urgent or emergent surgeries require communication between the patient’s cardiologist, anesthesiologist, and the surgical team. However, most guidelines recommend that, for these procedures which cannot be delayed, if the thienopyridine must be stopped it should be stopped as close to surgery as possible and re-started as soon as possible postoperatively, and aspirin should be continued if at all possible [36]. In cardiac surgery, the preoperative use of aspirin has resulted in greater blood loss and need for reoperation, but no increase in mortality, and is in fact associated with an increased saphenous vein graft patency rate [10].


            If and when cangrelor is available in the US, it will also provide the option of switching from clopidogrel to cangrelor 1 week preoperatively and thereby continuing DAPT until 1 day preoperatively, because of cangrelor’s rapid offset.

   C. Percutaneous valvular therapy

      1. Aortic valvuloplasty

        Percutaneous valvuloplasty leads to at least a 50% reduction in gradient in more than 80% of cases. Complications are relatively infrequent, including femoral artery laceration in up to 10% of patients, stroke in 1%, and a less than 1% incidence of cardiac fatality. Contraindications to aortic balloon valvuloplasty are significant PVD and moderate or greater aortic insufficiency. Aortic insufficiency usually increases during valvuloplasty. However, the acute development of severe aortic regurgitation can lead to pulmonary congestion and possibly death. Restenosis can occur as early as 6 months after the procedure and nearly all patients will have restenosis by 2 years. The most common indication for percutaneous aortic valvuloplasty is currently to temporarily improve poor left ventricular function in order to allow AVR.

      2. Mitral valvuloplasty

        Percutaneous mitral valvuloplasty (PMC) has been performed for 30 years as an alternative to surgery for patients with rheumatic mitral stenosis. The factor leading to success with mitral valvuloplasty is proper patient selection. Absolute contraindications to mitral valvuloplasty include:

        a. a known left atrial (LA) thrombus, or a recent embolic event within the preceding 2 months

        b. severe cardiothoracic deformity

        c. bleeding abnormality.

        Relative contraindications include:

        a. significant mitral regurgitation

        b. pregnancy

        c. concomitant significant aortic valve disease

        d. significant CAD

        All patients must undergo transesophageal echocardiography (TEE) to exclude LA thrombus.

          The procedure is reported to be successful in 85% to 99% of cases. Risks of percutaneous mitral commissurotomy include a procedural mortality of 0% to 3%, hemopericardium in 0.5% to 12% of patients, systemic embolism in 0.5% to 5%, and failure of the inter-atrial septum to close completely. Severe mitral regurgitation occurs in 2% to 10% of procedures and may require emergent surgery. Restenosis rates depend on the amount of calcium on the mitral valve commissures [37].

      3. Percutaneous valve replacement and repair

        Surgical valve replacement/repair is still the treatment of choice for stenotic aortic valves and regurgitant mitral valves when the surgical morbidity and mortality are not prohibitive. The first catheter-based alternative to surgical valve replacement was percutaneous pulmonic valve replacement. Success in this procedure led to similar procedures on the aortic and mitral valves. These percutaneous procedures are performed under general anesthesia with fluoroscopic and echocardiographic guidance. The results in high-risk patients have been promising, and the devices are now being tested in a lower risk group, as a true alternative to surgery [38]. Retrograde, antegrade, and transapical approaches to the aortic valve are used. For patients with severe vascular disease, the transapical approach using a small thoracotomy incision may be most suitable. This approach requires that general anesthesia be administered to a patient with critical aortic stenosis and may pose particular challenges for the anesthesiologist.

          The percutaneous approach for MR includes techniques to replace and to repair the mitral valve [39]. Two approaches have been used. The first involves placement of a device within the coronary sinus. This device can then be shortened, decreasing the size of the mitral annulus and the amount of MR, similar to a surgically placed annuloplasty ring. The second approach uses percutaneous suturing of the mitral leaflets with the MitraClip® (Evalve, Menlo Park, CA). A report on 107 patients described procedural success in 74% with a 9% rate of major but not lethal adverse events in a high-risk cohort. Trials are currently comparing the device to surgical repair. Both temporary and permanent mitral valve implantations have been attempted experimentally.

          As this field expands, the role of the cardiac anesthesiologist in the catheterization laboratory for these complex procedures will likely expand [30].

VI. Management of preoperative medications

   A. b-Adrenergic blockers. β-Adrenergic blockers are used commonly for the treatment of hypertension, stable and unstable angina, as well as MI. These drugs can also be used to treat SVT, including that due to pre-excitation syndromes, and the manifestations of systemic disease ranging from hyperthyroidism to migraine headaches. β-Blocker therapy is beneficial in the perioperative period, and the magnitude of the benefit is directly proportional to the patient’s cardiac risk [40]. Further, abrupt withdrawal of β-blockers can lead to a rebound phenomenon, manifest by nervousness, tachycardia, palpitations, hypertension, and even MI, ventricular arrhythmias, and sudden death. Many authors have found that preoperative treatment with β-blocking agents reduces perioperative tachycardia and lowers the incidence of ischemic events. [10,40]. Therefore, administration of β1 selective blockers should continue or be instituted in patients at risk for ischemic heart disease and without systolic heart failure or heart block. Continuation of β-blockade intraoperatively and postoperatively is essential to avoid rebound phenomenon.

   B. Statins (HMG-CoA inhibitors). Statins are used chronically to reduce the levels of low- density lipoproteins. However, they have also been shown to slow coronary artery plaque formation, increase plaque stability, improve endothelial function, and exhibit antithrombogenic, anti-inflammatory, antiproliferative, and leukocyte-adhesion-limiting effects. All of these effects would be expected to reduce both short- and long-term cardiovascular morbidity. Several large recent retrospective studies, the most recent by Lindenauer et al., have shown that preoperative statin use resulted in a significant reduction in postoperative mortality from 3.05% to 2.13% [41].

   Because all of these studies are retrospective and recorded only the patients taking statins during hospitalization, we have no indication of the duration of statin use needed to provide a beneficial effect or whether discontinuing statins several days preoperatively will reduce their protective effect. However, until more is known, it would be wise to continue statins preoperatively in those patients already taking the drugs, recognizing the small incremental risks of hepatotoxicity and rhabdomyolysis.

   C. Anticoagulant and antithrombotic medication

      1. Warfarin—approaches to preoperative therapy for patients taking chronic warfarin for (a) AF, (b) mechanical prosthetic heart valve, or (c) DVT/pulmonary embolus were recently reviewed by Watts and Gibbs. A simple but comprehensive approach, based on their recommendations, is shown in Tables 3.12 to 3.14.

Table 3.12 Preoperative anticoagulation management for chronic AF

Table 3.13 Management of preoperative anticoagulation for mechanical prosthetic heart valve

Table 3.14 Preoperative anticoagulation management for venous thromboembolism

      2. Dibigatran is a potent, non-peptide small molecule that reversibly inhibits both free and clot-bound thrombin. It has been approved for stroke prevention in patients with AF. Though peak effect occurs in 2 to 4 hrs after administration, its estimated half-life is 15 hrs with normal renal function. Based on the pharmacokinetics, in patients with normal renal function (eGFR >50 cc/min) discontinuation of two doses results in a decrease in the plasma level to about 25% of baseline and discontinuation of four doses will decrease the level to about 5% to 10% [42].

      3. Antithrombotic and antiplatelet therapy with agents such as clopidogrel (Plavix), cilostazol (Pletal), or combinations of agents should be stopped, if possible, 1 week preoperatively. Because of a concern for longer duration of action, ticlopidine (Ticlid) should be discontinued 2 wks preoperatively, and Fondaparinux (Arixtra) 1 mo preoperatively, using other agents as a bridge to surgery, if needed. Glycoprotein IIb/IIIa Inhibitors—(eptifibatide, tirofiban, abciximab) should be stopped approximately 48 hrs preoperatively.

   D. Antihypertensives

Preoperatively, chronic antihypertensive medications should usually be continued until the morning of surgery, and be begun again as soon as the patient is hemodynamically stable postoperatively. Continuation of β-blockers and α-2 agonists until the morning of surgery are particularly important because of the risks of rebound hypertension with sudden withdrawal of these drugs. In contrast, patients receiving ACE inhibitors and angiotensin II receptor blockers appear to be particularly prone to perioperative hypotension, so several authors recommend holding these agents the morning of surgery but re-starting them as soon as the patient is euvolemic postoperatively [43].


   E. Antidysrhythmics

Preoperative patients may require any of a large number of oral antidysrhythmic agents, including amiodarone, or calcium channel blockers. Therapy for ventricular dysrhythmias should be continued perioperatively.

Complete preoperative evaluation and proper premedication, including especially the use of β-blockade in appropriate patients with good ventricular function, smooth the patient’s transition into the operating room and may reduce the incidence of perioperative ischemia in susceptible patients.


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